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Mucins Help to Avoid Alloreactivity at the Maternal Fetal Interface
During gestation, many different mechanisms act to render the maternal immune system tolerant to semi-allogeneic trophoblast cells of foetal origin, including those mediated via mucins that are expressed during the peri-implantation period in the uterus. Tumour- associated glycoprotein-72 (TAG-72) e...
Autores principales: | , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Hindawi Publishing Corporation
2013
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3705806/ https://www.ncbi.nlm.nih.gov/pubmed/23864879 http://dx.doi.org/10.1155/2013/542152 |
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author | Redzovic, Arnela Laskarin, Gordana Dominovic, Marin Haller, Herman Rukavina, Daniel |
author_facet | Redzovic, Arnela Laskarin, Gordana Dominovic, Marin Haller, Herman Rukavina, Daniel |
author_sort | Redzovic, Arnela |
collection | PubMed |
description | During gestation, many different mechanisms act to render the maternal immune system tolerant to semi-allogeneic trophoblast cells of foetal origin, including those mediated via mucins that are expressed during the peri-implantation period in the uterus. Tumour- associated glycoprotein-72 (TAG-72) enhances the already established tolerogenic features of decidual dendritic cells with the inability to progress towards Th1 immune orientation due to lowered interferon (IFN)-γ and interleukin (IL)-15 expression. Mucine 1 (Muc 1) supports alternative activation of decidual macrophages, restricts the proliferation of decidual regulatory CD56(+) bright natural killer (NK) cells, and downregulates their cytotoxic potential, including cytotoxic mediator protein expression. Removing TAG-72 and Muc 1 from the eutopic implantation site likely contributes to better control of trophoblast invasion by T cells and NK cells and appears to have important immunologic advantages for successful implantation, in addition to mechanical advantages. However, these processes may lead to uncontrolled trophoblast growth after implantation, inefficient defence against infection or tumours, and elimination of unwanted immunocompetent cells at the maternal-foetal interface. The use of mucins by tumour cells to affect the local microenvironment in order to avoid the host immune response and to promote local tumour growth, invasion, and metastasis confirms this postulation. |
format | Online Article Text |
id | pubmed-3705806 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2013 |
publisher | Hindawi Publishing Corporation |
record_format | MEDLINE/PubMed |
spelling | pubmed-37058062013-07-17 Mucins Help to Avoid Alloreactivity at the Maternal Fetal Interface Redzovic, Arnela Laskarin, Gordana Dominovic, Marin Haller, Herman Rukavina, Daniel Clin Dev Immunol Review Article During gestation, many different mechanisms act to render the maternal immune system tolerant to semi-allogeneic trophoblast cells of foetal origin, including those mediated via mucins that are expressed during the peri-implantation period in the uterus. Tumour- associated glycoprotein-72 (TAG-72) enhances the already established tolerogenic features of decidual dendritic cells with the inability to progress towards Th1 immune orientation due to lowered interferon (IFN)-γ and interleukin (IL)-15 expression. Mucine 1 (Muc 1) supports alternative activation of decidual macrophages, restricts the proliferation of decidual regulatory CD56(+) bright natural killer (NK) cells, and downregulates their cytotoxic potential, including cytotoxic mediator protein expression. Removing TAG-72 and Muc 1 from the eutopic implantation site likely contributes to better control of trophoblast invasion by T cells and NK cells and appears to have important immunologic advantages for successful implantation, in addition to mechanical advantages. However, these processes may lead to uncontrolled trophoblast growth after implantation, inefficient defence against infection or tumours, and elimination of unwanted immunocompetent cells at the maternal-foetal interface. The use of mucins by tumour cells to affect the local microenvironment in order to avoid the host immune response and to promote local tumour growth, invasion, and metastasis confirms this postulation. Hindawi Publishing Corporation 2013 2013-06-20 /pmc/articles/PMC3705806/ /pubmed/23864879 http://dx.doi.org/10.1155/2013/542152 Text en Copyright © 2013 Arnela Redzovic et al. https://creativecommons.org/licenses/by/3.0/ This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Review Article Redzovic, Arnela Laskarin, Gordana Dominovic, Marin Haller, Herman Rukavina, Daniel Mucins Help to Avoid Alloreactivity at the Maternal Fetal Interface |
title | Mucins Help to Avoid Alloreactivity at the Maternal Fetal Interface |
title_full | Mucins Help to Avoid Alloreactivity at the Maternal Fetal Interface |
title_fullStr | Mucins Help to Avoid Alloreactivity at the Maternal Fetal Interface |
title_full_unstemmed | Mucins Help to Avoid Alloreactivity at the Maternal Fetal Interface |
title_short | Mucins Help to Avoid Alloreactivity at the Maternal Fetal Interface |
title_sort | mucins help to avoid alloreactivity at the maternal fetal interface |
topic | Review Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3705806/ https://www.ncbi.nlm.nih.gov/pubmed/23864879 http://dx.doi.org/10.1155/2013/542152 |
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